You're incredibly wrong. Go re read what PZ says, and what Kurtzweil says. Kurtweil says that we can get to the end of system by looking at the information contained in the genome.
You don't have to be able simulate electrons in a transistor to get that to work, but you do need to know how the system works. You can shortcut the electron simulation if you can describe the system.
PZ points out very, very clearly that we do NOT know how protein systems work and interact. The existence of Fold it, the protein folding game is testament to that problem. You are certainly correct that the presumptive brain model will not directly simulate the proteins, and PZ never says it does. But the problem is that we don't KNOW how to simulate them.
PZ says:
Let me give you a few specific examples of just how wrong Kurzweil's calculations are. Here are a few proteins that I plucked at random from the NIH database; all play a role in the human brain.
First up is RHEB (Ras Homolog Enriched in Brain). It's a small protein, only 184 amino acids, which Kurzweil pretends can be reduced to about 12 bytes of code in his simulation. Here's the short description.
MTOR (FRAP1; 601231) integrates protein translation with cellular nutrient status and growth signals through its participation in 2 biochemically and functionally distinct protein complexes, MTORC1 and MTORC2. MTORC1 is sensitive to rapamycin and signals downstream to activate protein translation, whereas MTORC2 is resistant to rapamycin and signals upstream to activate AKT (see 164730). The GTPase RHEB is a proximal activator of MTORC1 and translation initiation. It has the opposite effect on MTORC2, producing inhibition of the upstream AKT pathway (Mavrakis et al., 2008).
Got that? You can't understand RHEB until you understand how it interacts with three other proteins, and how it fits into a complex regulatory pathway. Is that trivially deducible from the structure of the protein? No. It had to be worked out operationally, by doing experiments to modulate one protein and measure what happened to others. If you read deeper into the description, you discover that the overall effect of RHEB is to modulate cell proliferation in a tightly controlled quantitative way. You aren't going to be able to simulate a whole brain until you know precisely and in complete detail exactly how this one protein works.
PZ basically spent his entire article saying that we don't understand how the biologic equivalent of electrons in a semi conductor work, and it's really, really tough to figure out. Transistors are simple. Proteins are not. The amount of computational power that can be put into simulating a single protein is staggering. And until you work out shortcuts for each protein in the system, you can't just jump to your proposed end game. That's the point.